Kaira Bhutada
Pronouns: she/her
Research Mentor(s): Rahasudha Kannan
Research Mentor School/College/Department: Biomedical Engineering; Periodontal Medicine / Engineering
Program:
Authors: Kaira Bhutada, Rahasudha Kannan
Session: Session 7: 4:40 pm – 5:30 pm
Poster: 31
Abstract
Macrophages, professional phagocytic cells, engulf dead or dying (apoptotic) cells in efferocytosis. Blocking efferocytosis can impair bone repair, signifying the crucial role of macrophages and efferocytosis in healing. However, the specific contributions of macrophage efferocytosis in bone repair are still unclear. Efferocytic macrophages are known to secrete various factors that facilitate repair and inflammation resolution. After macrophages clear apoptotic bone cells, they upregulate CCL2, which may play a role in mesenchymal stem/progenitor cell recruitment. This study aims to understand the specific role of macrophage efferocytosis and CCL2 in early spontaneous bone healing using an ulna stress fracture model in wild-type (WT) and CCR2-/- (CCR2 KO) mice. Blinded microCT analysis of mineralizing calluses seven days post-injury was performed to obtain trabecular bone parameters: bone volume (BV), bone volume percentage (BV/TV), trabecular number (Tb.N), trabecular thickness (Tb.Th), trabecular spacing (Tb.Sp), and tissue mineral density (TMD). This study hypothesizes that BV, BV/TV, Tb.N, Tb.Th, and TMD will decrease, and that Tb.Sp will increase in the CCR2-/- mice compared to wild type mice. The results of this analysis will provide further insight into the role of CCL2 signaling in early bone repair.
